Premature birth leaves many infants with severe respiratory problems, as the lungs are one of the last organs to develop in the womb. Babies that are born early often struggle to take in enough oxygen because of their underdeveloped lungs, leading to chronic lung disease which can last into adulthood. Currently doctors administer steroids to try and help the lungs develop, along with a gas which has a high concentration of oxygen. However a more effective new treatment could be on the horizon following a recent study. Work on mouse embryos has led to the discovery that calcium receptors (CaR), are responsible for coordinating the development of structures in the lungs, acting like a ‘mechanical switch’. A greater understanding of the role of these receptors in lung development could lead to existing medicines that affect calcium levels being developed and modified for use in progressing lung development. - Journal of Physiology DOI: 10.1113/jphysiol.2008.161687, 15 December 2008

A study in mice has shown how an enzyme, PLCg1, could be responsible for cancer cells spreading from original tumors around the body. The ability of cells to migrate from an original tumor is one of the biggest problems in the treatment of cancer. Once the cells begin to spread, then the cancer is much more difficult to treat. If the internal organs become overwhelmed by tumors, then the cancer often becomes untreatable and fatal. The team made a huge breakthrough in this field when they discovered that PLCg1 is necessary for breast cancer cells to spread from the original tumor and form secondary tumors elsewhere. They blocked PLCg1 in mice and saw that the breast cancer cells no longer spread into the lungs; however it was noted there was little effect on the original tumor. Along with the mice studies, the team also took samples from human breast cancer patients and found higher levels of PLCg1 in the secondary tumors of half the patients. This strongly suggests that medicines which block PLCg1 may have potential in the treatment of tumor spread in humans. - Cancer Research DOI: 10.1158/0008-5472.CAN-08-1181, 15 December 2008

Scientists have shown that by blocking a specific protein in mice, the formation of scar tissue in the heart can be reduced. Non-fatal heart attacks starve the heart muscle of oxygen, causing collagen to build up in a process called fibrosis. This leads to the formation of scar tissue which can permanently affect the hearts ability to pump blood. Researchers targeted a specific protein – sFRP2 – to see if it was responsible for the chain reaction that causes collagen formation. They genetically blocked sFRP2 in mice, and found that those lacking the protein had far less scarring after artificial heart attacks were induced. The findings are promising, but the genetic block on sFRP2 cannot be applied in humans. Results could however lead to the development of a medicine that could reduce fibrosis in humans in the hours after a heart attack. Fibrosis and scar tissue formation is not just a problem in the heart; it is also seen in other diseases such as liver and lung disease. If a medicine is found that can reduce fibrosis, then there could be many more medical applications. - Nature Cell Biology DOI: 10.1038/ncb1811, 14 December 2008

Cancer researchers may have underestimated the power of some cancers to spread and cause new tumors. Scientists have found that just one skin cancer cell was often enough to generate a whole new tumor. Normally the ability of a single cell to generate a new tumor is tested by injecting large quantities of the cancer cell into mice with weakened immune systems and counting how many tumors emerge. However, the scientists believed this approach was flawed, because the mice still had some immunity to these human cancer cells. So they severely weakened the immune systems of the mice before injected them with melanoma (skin cancer) cells. They found that the number of cells forming tumors was 250,000 times more than before. When single melanoma cells were used, they discovered that around one quarter went on to generate new tumors. Dr Sean Morrison, who led the latest work, said "As far as we know, this is the first time anyone has been able to show that individual cells from human cancers can efficiently form tumors." This shows the importance of fundamental research into how cancers develop and the team has called for researchers to improve their tests to see if other cancers are equally potent. - Nature DOI: 10.1038/nature07567, 4 December 2008

Scientists have cured mice with a similar genetic defect to human sickle cell, by inserting a gene into their blood-forming cells. The mice were as well as after treatment as normal mice, and their symptoms were alleviated. Sickle cell disease is caused by a genetic defect which causes red blood cells to deform with the result that they can no longer transport oxygen around the body properly, leading to severe tiredness. In acute attacks they can even get stuck in blood vessels, leading to severe pain. The only permanent cure is a bone marrow transplant but there is a shortage of compatible donors. The gene inserted into the mice cells is found in the red blood cells of fetuses, and usually disappears soon after birth. When inserted into adult cells responsible for producing red blood cells, the gene induced production of a different protein. Months after introducing the altered blood-forming cells, the mice continued to produce this protein. While the mouse experiments should lead to treatments for human patients, there are technical barriers. For instance, it is easier to insert genes into mouse cells than into human cells, with a higher rate of success. However, the group is working with different cells to develop better methods to take this gene therapy treatment into humans. - Molecular Therapy DOI: 10.1038/mt.2008.259, 2 December 2008

A protein which plays an active role in preventing some types of cancer has now been implicated in causing others. Studies in mice and rats have shown that glycogen synthase kinase 3 (GSK3) is responsible for promoting mixed-linkage leukemia, which accounts for 3 in 4 cases of the disease in children. GSK3 had previously been ignored as a possible drug target because of its association with preventing cancer. But scientists confirmed the discovery by showing that inhibiting the protein in animal tests led to lower rates of leukemia. The findings may prompt research into drugs which can safely block GSK3 in humans, without running too great a risk of encouraging the appearance of other cancers which the protein successfully inhibits. - Nature online DOI: 10.1038/nature07284, 17 September 2008

A study in mice has confirmed the existence of stem cells which can regenerate lost muscle fibre. Stem cells are sometimes known as ‘master’ cells for their ability to not only replicate themselves, but also turn into many other types of cell. This power gives scientists hope that they can be used to replace tissue lost through disease or injury. Previously, researchers had found it difficult to get muscle stem cells to repair damage, or to isolate precisely which cells were doing the repairing. The new experiment confirms that the stem cells are found in the ‘basal lamina’ which surrounds muscles. And by tagging individual cells with a fluorescent protein, scientists could track which cells were creating new muscle fibers. Now that scientists have a clearer understanding of how to find these muscle stem cells they may find it easier to manipulate them in treatments for diseases such as muscular dystrophy. - Nature online DOI: 10.1038/nature07384, 17 September 2008

Scientists have known for a while that changing the activity of specific genes in a mouse’s brain can make it overly timid or brave, as they appear to control ‘fear’. Now, a similar experiment has shown that the gene stathmin controls how worried mouse mothers become about their pups. In the recent work, researchers inactivated stathmin in female mice. The animals were slower to retrieve their pups when they were removed from their nests, and were more likely to build nests in exposed areas, compared to normal mice. This was despite stockpiling food as quickly, and being able to smell as well as normal rats - showing that they weren’t simply lazy or had their senses impaired. Stathmin has its effect in the amygdala, an area of the brain common to humans. Other experiments had shown that when the relevant area of the amygdala is damaged, the effect on parental activity is similar. - Proceedings of the National Academy of Sciences online DOI: 10.1073/pnas.0807507105, 15 September 2008

A new treatment, tested on rats, could help to prevent ‘chemo brain’ – the generic term for post-chemotherapy problems including memory loss, difficulty concentrating, and other cognitive issues in cancer patients. Doctors were unsure whether the condition is due to chemotherapy or the cancer, but in either case it can lead to a severe reduction in quality of life. Scientists gave rats the chemotherapy drugs adriamycin (ADR) and cytoxan (CTX), and found that they performed worse on memory tests. This suggests that chemo brain is caused by chemotherapy, as the rats did not have cancer. They also gave some of the rats N-acetyl cysteine (NAC), a powerful anti-oxidant, and found that those rats showed fewer chemo brain symptoms. The safety of NAC for cancer patients now needs to be established before the treatment can be used in humans. - Metabolic Brain Disease online DOI: 10.1007/s11011-008-9100-y, 9 September 2008

A protein which plays an active role in preventing some types of cancer has now been implicated in causing others. Studies in mice and rats have shown that glycogen synthase kinase 3 (GSK3) is responsible for promoting mixed-linkage leukemia, which accounts for 3 in 4 cases of the disease in children. GSK3 had previously been ignored as a possible drug target because of its association with preventing cancer. But scientists confirmed the discovery by showing that inhibiting the protein in animal tests led to lower rates of leukemia. The findings may prompt research into drugs which can safely block GSK3 in humans, without running too great a risk of encouraging the appearance of other cancers which the protein successfully inhibits. - Nature online DOI: 10.1038/nature07284, 17 September 2008

A study in mice has confirmed the existence of stem cells which can regenerate lost muscle fibre. Stem cells are sometimes known as ‘master’ cells for their ability to not only replicate themselves, but also turn into many other types of cell. This power gives scientists hope that they can be used to replace tissue lost through disease or injury. Previously, researchers had found it difficult to get muscle stem cells to repair damage, or to isolate precisely which cells were doing the repairing. The new experiment confirms that the stem cells are found in the ‘basal lamina’ which surrounds muscles. And by tagging individual cells with a fluorescent protein, scientists could track which cells were creating new muscle fibers. Now that scientists have a clearer understanding of how to find these muscle stem cells they may find it easier to manipulate them in treatments for diseases such as muscular dystrophy. - Nature online DOI: 10.1038/nature07384, 17 September 2008

Scientists have known for a while that changing the activity of specific genes in a mouse’s brain can make it overly timid or brave, as they appear to control ‘fear’. Now, a similar experiment has shown that the gene stathmin controls how worried mouse mothers become about their pups. In the recent work, researchers inactivated stathmin in female mice. The animals were slower to retrieve their pups when they were removed from their nests, and were more likely to build nests in exposed areas, compared to normal mice. This was despite stockpiling food as quickly, and being able to smell as well as normal rats - showing that they weren’t simply lazy or had their senses impaired. Stathmin has its effect in the amygdala, an area of the brain common to humans. Other experiments had shown that when the relevant area of the amygdala is damaged, the effect on parental activity is similar. - Proceedings of the National Academy of Sciences online DOI: 10.1073/pnas.0807507105, 15 September 2008

A new treatment, tested on rats, could help to prevent ‘chemo brain’ – the generic term for post-chemotherapy problems including memory loss, difficulty concentrating, and other cognitive issues in cancer patients. Doctors were unsure whether the condition is due to chemotherapy or the cancer, but in either case it can lead to a severe reduction in quality of life. Scientists gave rats the chemotherapy drugs adriamycin (ADR) and cytoxan (CTX), and found that they performed worse on memory tests. This suggests that chemo brain is caused by chemotherapy, as the rats did not have cancer. They also gave some of the rats N-acetyl cysteine (NAC), a powerful anti-oxidant, and found that those rats showed fewer chemo brain symptoms. The safety of NAC for cancer patients now needs to be established before the treatment can be used in humans. - Metabolic Brain Disease online DOI: 10.1007/s11011-008-9100-y, 9 September 2008

Scientists have managed to restore fur growth to dilapidated mice by using a single molecule, laminin-511. The news could come as a relief to the hundreds of millions of people worldwide who suffer from hair loss or alopecia. Researchers found that laminin-511 works as a molecular messenger in the skin. It operates between the upper and lower layers of the skin, encouraging individual follicles to begin re-growing hair. In this respect it differs from conventional hair-loss treatments, which tend to only slow the process, rather than actively reverse it. Mice given laminin-511 injections re-grew their fur to half the thickness of their normal coat. As noted by the scientists, although hair-loss is not a life-threatening condition, it can be traumatic, especially for women or chemotherapy patients. If the treatment works as well in clinical trials as it does in mice, it could be a few years from being on the market. - Genes and Development DOI: 10.1101/gad.1689908, August 2008

While the predicted H5N1 ‘bird flu’ epidemic has yet to strike, new tests on ferrets have revealed that we could be at risk from another variant – H9N2. If the findings are borne out by further research, they could provide a crucial early-warning for the development of a treatment and/or vaccine against the disease. The H5N1 virus is much feared because, although it cannot be transmitted from human to human, the disease is severe when passed from an animal. There are worries that if the virus mutates so that it becomes able to be transmitted from human to human, it could cause an epidemic. The new research shows that H9N2 is only a few mutations from becoming as dangerous as H5N1 in humans, as our immune systems are fairly similar to the ferrets used in the experiment. One reassuring aspect of the research was that it seemed the virus was difficult to transmit through the air, unlike H5N1. This should make H9N2 difficult to catch, even if it does become as virulent as H5N1. - PLoS ONE DOI: 10.1371/journal.pone.0002923, 13 August 2008

Scientists working with rhesus macaques have discovered that there may be an unexpected interplay between our senses of hearing and sight. Traditional models of our sensory function suggest that our brain is very hierarchical, with different neural areas being responsible for different senses and reporting to a central processing area – but the new work suggests there might be room for more sideways interaction. The research builds on findings that there are some neurons directly connecting the visual and the auditory areas of the brain. Researchers found that when monkeys were presented with a strong visual stimulus, having a simultaneous sound coming from the same spot didn’t make any difference to how the monkeys perceived the stimulus. If the visual stimulus was quite weak, the simultaneous sound increased the speed of the monkeys’ perception by 5-10%, making up for the lack of visual cues. The work could have important implications for future work into the senses, and further understanding of neurology. - BMC Neuroscience DOI: 10.1186/1471-2202-9-79, 12 August 2008

A new treatment has been shown to dramatically lower cholesterol in mice, rats, and monkeys. The therapy could be a major improvement on current cholesterol-busting methods, as unlike most drugs, it is based on a type of RNA (a chemical relative of DNA) so it will have fewer side-effects. The treatment uses a molecule of siRNA (small interfering RNA) to throw a spanner in the works of the production of a protein called PCSK9, which usually raises levels of LDL (or ‘bad’) cholesterol. All proteins rely on RNA for their translation from DNA genes, and siRNA can be used to interfere with that RNA. When animals were given the treatment, they showed a reduction of over half in their levels of PCSK9, resulting in a reduction in cholesterol levels of up to two-thirds. Given its success in animal tests, the technique could soon be used in humans. - Proceedings of the National Academy of Sciences, online DOI: 10.1073/pnas.0805434105, 11 August 2008

Scientists have successfully created a mouse which cannot become fat, by tinkering with the genetics of its hormones. The research could eventually lead to a treatment for obese humans, helping to avoid secondary conditions such as diabetes, cardiac disease, and sleep apnea. The mice were created by modifying them so that an area of their brains called the hypothalamus – which controls hunger, thirst, and other bodily functions – cannot produce a chemical called GABA. Without GABA, the mice burned energy at a much faster rate than normal mice. Because of this, even when they were given more food, they put on much less weight than mice which produced GABA. Almost one-in-ten of the global population is obese, with the figure being closer to one-in-three for the United States. If the findings lead to a drug treatment, it could result in significant financial savings in healthcare for obese individuals further down the line. - Nature Neuroscience DOI: 10.1038/nn.2167, 10 August 2008

Scientists working with mice have artificially created large quantities of useful platelets for the first time. The work could have major implications treating people with low platelet counts, such as anemics and chemotherapy patients. Platelets are essential in blood clotting – without them, people can bleed to death from quite minor wounds. Previously, platelets had only been grown artificially along with other types of blood cells. These platelets don’t clot as well as real platelets, due to a change in their surface proteins. The researchers have now succeeded in creating stem cells that only produce platelets. They have made sure they clot properly by removing an enzyme which affects the surface proteins. If the technique proves commercially viable, it could be superior to traditional methods of filtering platelets from donated blood, as it avoids the risk of infection from contaminated blood. - Journal of Experimental Medicine DOI: 10.1084/jem.20071482, 28 July 2008

Much of the damage that occurs following an influenza infection isn’t caused by the virus itself, but by the body’s immune system reacting against it. But a new experiment in mice has shown that it might be possible to dampen this immune response without affecting how well it clears the virus, which could reduce deaths and recovery times from the disease. Immune responses in the lungs are partly subdued by the CD200 receptor being active. However, the influenza virus blocks the CD200 molecule, meaning that the immune response stays active long after the virus itself is cleared. Scientists gave mice an artificial molecule which mimicked the effects of CD200. When infected with the ‘flu, treated mice lost less weight, had less inflammation in their lungs, and recovered quicker. As well as helping to treat seasonal ‘flu, any new treatment based on the findings could also form part of the defense against a global ‘flu pandemic. - Nature Immunology DOI: 10.1038/ni.1637, 27 July 2008

A treatment for pancreatic cancer could be on the way after successful experiments in mice. Finding drugs which might tackle pancreatic cancer is a high priority; 60,000 people are diagnosed with it each year in Europe alone, but only one-in-twenty of those will survive more than five years with the disease. The new work focuses on a treatment known as chemoprevention gene therapy (CGT). It combines using a drug (mda-7/IL-24) with a dietary supplement (perillyl alcohol). The perillyl alcohol acts as an enabler, and stops the cancer cells from blocking the effect of the primary drug. Mice which received the treatment not only developed fewer tumors initially, but their existing tumors also shrank. Researchers will now be investigating whether the technique works in humans, too, by beginning clinical trials of the treatment. - Molecular Cancer Therapeutics DOI: 10.1158/1535-7163.MCT-08-0245, July 2008

GERD – gastro-esophageal reflux disease – is a common cause of heartburn and respiratory problems. It occurs when stomach acids make their way up the esophagus (gullet), and then back down into the windpipe. New research in mice has shown how suffering from GERD could also increase your risk of developing asthma. Scientists have been aware of the link for some time, but the actual mechanism was previously unclear. In the research, healthy mice had small amounts of stomach acid placed into their lungs over two months. The mice then had slightly different immune responses to allergens compared to normal mice, contributing to a higher sensitivity – much like asthma in humans. Although there is no definitive cure for GERD, it is treatable, which means that many cases of asthma might be prevented by early diagnosis of GERDs. - European Journal of Clinical Investigation DOI: 10.1111/j.1365-2362.2008.01976.x, 17 July 2008

Anti-impotence drugs such as Viagra and Levitra could be crucial for treating brain cancer, according to an experiment carried out in rats. Brain cancers account for more than one in 50 of all cancer deaths, but over a fifth of cases in children. Present treatments are hampered by the presence of the blood-brain tumor barrier, which stops drugs from entering tumors, just as the normal blood-brain barrier prevents chemicals from entering the brain. Researchers found that when they administered the anti-impotence drugs to rats with brain tumors, the blood-brain tumor barriers opened up, allowing more of the anti-cancer drug to reach the tumor. Some of the treated rats survived more than 20% longer than animals receiving just the anti-cancer drugs, which may spur on research leading to trials of the technique in humans. - Brain Research, advanced online DOI: 10.1016/j.brainres.2008.06.122 , 14 July 2008

In a finding that could be key to future research in contraception and fertility treatments, scientists have found a gene in mice which controls ovulation. Blocking the gene, known as Lrh1, could prevent ovulation and provide a fool-proof alternative to the contraceptive pill, while boosting it could help couples who are unable to conceive. Researchers made the discovery by genetically modifying some mice to lack Lrh1. They found that the resulting females had slightly different levels of hormones, which prevent the complex series of events that leads to an egg maturing in the ovaries. If the gene is missing, the eggs fail to appear, making the mice sterile. Blocking the gene’s activity in humans could give a side-effect-free form of contraception, but it will require a lot of further research before that could hit the market. - Genes and Development DOI: 10.1101/gad.472008, July 2008

If it wasn’t bad enough that rotavirus infections cause millions of cases of childhood diarrhoea – leading to half a million deaths worldwide each year – new research in mice has found that the virus could also trigger a quicker onset of diabetes. Type II diabetes occurs in middle- and old-age, and is heavily influenced by diet and environmental factors. Type I diabetes often strikes younger people, and occurs when their immune systems destroy their insulin-producing cells. The new research shows that, depending on how old the animal is at time of infection, exposure to rotavirus can make the destruction of those cells much more rapid. The interplay seems to be quite complex – sometimes infection can actually delay the onset of diabetes – but the work is an important step in understanding diabetes type I and other auto-immune diseases. - Journal of Virology DOI: 10.1128/JVI.00597-08, July 2008

Over 30 million people live with AIDS worldwide, and there is still no cure. This makes preventing transmission of the HIV agent a top priority in combating the pandemic – and new research in monkeys has implicated parasitic worms in the ability of the disease to take hold. Scientists infected one group of monkeys with parasitic helminths, a type of worm, and kept another group free of infection, before being exposed to the monkey version of HIV. The worm-infected monkeys were 17-times more susceptible to being infected by HIV. Once they were infected, they also had more viruses in their blood – indicating that they might succumb to AIDS quicker. The findings could be vital in helping prevent the spread of HIV in developing countries, as parasitic worms are often an endemic problem there. If the worms can be fought, it could help in the battle against AIDS. - PLoS Neglected Tropical Diseases DOI: 10.1371/journal.pntd.0000265, 23 July 2008

If you’re constantly waking up in the middle of the night needing to use the bathroom, your brain might be as much to blame as your bladder – according to new research on rats. The findings could mean that bladder-associated insomnia should be treated with drugs that target specific brain areas. Researchers made the discovery by surgically narrowing the urinary tracts of rats, and monitoring the electrical activity in their brains – specifically, their Barrington’s nucleus, which is where the bladder reports to. They found that the Barrington’s nucleus became hyperactive, and in turn stimulated other parts of the rat’s brain, which may have caused sleep disturbances. The secondary effects disappeared when researchers surgically removed part of the Barrington’s nucleus. The work emphasizes the two-way interaction between the brain and the body, and paves the way for a better understanding of how that can lead to neurological problems. - Proceedings of the National Academy of Sciences, online DOI: 10.1073/pnas.0800969105, 21 July 2008

Scientists studying mice have discovered the proteins which regulate how the immune system responds to an infection by noroviruses. The most infamous type of norovirus is Norwalk, and as a group they are responsible for millions of gastroenteritis infections worldwide, often in closed communities such as cruise ships, hospitals, and prisons. When they created genetic ‘knock-out’ mice, which lacked the protein MDA-5, researchers noted that the animals were much more susceptible to infection and disease from noroviruses. A similar effect was found for the protein TLR3, but was less pronounced, leading scientists to believe TLR3 functions as a secondary sensor for the virus. The two proteins both work by detecting double stranded RNA, a rare form of nucleic acid that the noroviruses produce. If the same proteins have a similar effect in humans, the research could be a starting point for creating a treatment which kick-starts the immune response to the potentially fatal disease. - PLoS Pathogens DOI: 10.1371/journal.ppat.1000108, 18 July 2008

A successful experiment in mice has led researchers to suggest that it might be possible to use tiny magnetic nanoparticles to filter out errant ovarian cancer cells, preventing them from spreading and forming new tumors. Ovarian cancers are the fifth most common cause of cancer-related death in women, often caused by the secondary tumors that the new technique seeks to prevent. The treatment is based on a nanoparticle with a magnetic core, and covered in receptors which bind to molecules on the surface of stray cancer cells. When scientists injected the nanoparticles into the abdomens of mice affected by cancer, the magnetic particles bound to the cancer cell - Journal of the American Chemical society, online DOI: 10.1021/ja801969b, 9 July 2008

Memantine, a drug originally developed to treat Alzheimer’s Disease, could have an unexpected benefit in preventing brain damage in premature babies. One of the drug’s effects is to block a receptor in the brain known as NMDA. Experiments in rats have shown that effect could also stop periventricular leukomalacia (PVL), the death of brain cells following hypoxic ischemia (lack of oxygen or blood supply). PVL primarily affects premature babies, and can lead to cerebral palsy or other developmental syndromes. Scientists blocked NMDA receptors in rats, and found memantine prevents their over-activation that leads to PVL. Currently there are few effective therapies which can prevent PVL. Memantine doesn’t seem to cause any negative side-effects on the developing brain, so could potentially fill the treatment-gap. - Journal of Neuroscience DOI: 10.1523/JNEUROSCI.1702-08.2008, 25 June 2008

Recent research involving mice has given scientists hope that a vaccine against colonic cancer could be close to fruition. Work in the field has been dogged by the fact that it’s difficult to find a characteristic of cancer cells that is constant across different people, but still distinct from normal body tissues. The new work seems to have succeeded where others have failed by looking at a protein called guanylyl cyclase c (GCC). GCC is normally only found on the surface of the intestines, but is also expressed by nearly all colonic cancers. The cancers are most dangerous when they spread to other parts of the body, such as the lungs and liver. Scientists vaccinated mice against GCC to see if they could prevent that spread. Since the immune system doesn’t interact with the intestinal surface, normal body cells should be safe. Vaccinated mice had only a tenth of the number of tumors compared to unvaccinated mice, and they lived longer. With over half of the 1.2 million new colonic cancer patients every year dying of tumors that spread to the liver and lungs, the findings have the potential to save thousands of lives.- Journal of the National Cancer Institute, Advance Access DOI: 10.1093/jnci/djn178, 24 June 2008

Anesthetics provide vital relief during painful procedures, but new research conducted in mice suggests that they could paradoxically also cause pain after being administered. General anesthetics work by activating receptors in the brain which cause the parts of the organ responsible for consciousness to shut down. They also have other effects elsewhere in the body, including pain-sensing nerve cells (nocireceptors). Researchers found that one of the proteins that they affect in these cells, TRPA1, is the same channel protein which is opened by the extra-hot spice wasabi, along with other irritants. The pain and inflammation caused by these side-effects of anesthetics could increase recovery times from operations. The hope is that either new anesthetics can be developed which don’t cause pain, or the effect can be blocked; the hunt is already on for drugs which will interrupt the link between the anesthetics and pain receptors. - Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.0711038105, 23 June 2008

Scientists have long-suspected that the cause of Alzheimer’s Disease might be the build up of a type of protein, known as amyloid, into plaques in the brain. This theory is complicated by the fact that individuals with no symptoms of Alzheimer’s often have similar buildups, and are perfectly healthy. A new study in rats could explain the confusion. Researchers took samples of amyloid proteins from the brains of deceased patients, and injected them into the brains of the rats. The first thing they found was that the amyloid had to be in a soluble form to cause any symptoms. But by using antibodies to destroy specific sub-types of the amyloid protein, they found that only one of the three types of the protein did the damage. This led them to suggest that it could be the other two types of amyloid which cause the plaques in people without symptoms. Scientists can now focus on the one remaining type of amyloid to try and find why it is so destructive. - Nature Medicine online DOI: 10.1038/nm1782, 22 June 2008

The traditional model of measles infection, where the virus gains an initial foothold in the endothelial (surface) cells of the lungs and airways before spreading to the rest of the body, has been challenged by new research conducted in monkeys. A better understanding of the disease could help to cut death rates, which can reach one-in-ten in some developing countries. The new findings follow an experiment where the measles virus was mutated so that it couldn’t infect the airway endothelial cells. Under the traditional model, this would have meant that the virus couldn’t spread at all, but the research showed that it invaded the immune cells as a way of getting around the body. As well as being a potential killer, the measles virus is also being investigated for its ability to selectively kill cancer cells. The research could help scientists target the measles virus at tumors more accurately. - Journal of Clinical Research DOI: 10.1172/JCI35454, 20 June 2008

After successful experiments in mice, scientists believe they have found a molecule which can significantly reduce the risk of immune rejection of transplanted organs. The new findings could lead to a reduction in the amount of immunosuppressant drugs that transplant patients have to take, with the side-effects of those drugs including higher rates of cancer and infectious disease. The research team found that some types of a molecule known as HLA-G bind with immune cells known as dendritic cells (DCs). DCs normally play an integral part in the immune response against large foreign bodies, but are prevented from doing so by HLA-G. Mice which received skin grafts were much less likely to reject them after treatment with the molecule. As well as boosting the levels of HLA-G to prevent transplant rejection, the researchers believe there is a possibility that decreasing levels of the molecule could heighten the body’s sensitivity to tumors, opening up a new avenue in the fight against cancer. - Proceedings of the National Academy of Sciences, online DOI: 10.1073/pnas.0803341105, 11 June 2008

More Breast Cancer Genes Found

Researchers have uncovered five new genes which appear to be linked to breast cancer, and experiments in mice lead them to think one of them could be a prime candidate for drug treatments. The disease is one of the most common types of cancer worldwide, second only to lung cancer. The study looked at the role of a protein known as vascular endothelial growth factor (VEGF) in the mammary gland, which is associated with metastasis (the spread of cancerous cells from a tumor). After finding five genes which control the function of VEGF, scientists homed in on one in particular, tenascin-c. When tenascin-c was blocked, the mice in the study not only had less metastasis, but also had fewer initial tumors. The researchers believe that as well as being a target for drugs itself, studying the tenascin-c pathway could shed light on other ways of halting or slowing the progression of breast cancer. - Oncogene advance, online publication DOI: 10.1038/onc.2008.155, 26 May 2008

People suffering from the debilitating brain disorder, Alzheimer’s disease, have been given another potential treatment to look forward to. Scientists have successfully tested a vaccine against the disease in mice, which seems to protect the animals against both the symptoms and the causes of the disorder. The vaccine consisted of a genetically modified herpes virus that does not cause disease. Instead the virus made the proteins that build up into amyloid plaques which, when present in the brain, cause Alzheimer’s. The mouse immune system responded to the GM virus by mounting a response against the proteins, preventing them from building up in the brain. Mice receiving the treatment showed better mental ability and healthier brain tissue. The researchers hope to continue animal trials of the vaccine, with human trials expected to start in a few years time. - Molecular Therapy DOI: 10.1038/mt.2008.39, May 2008

Sugar Link to Fertility

An unexpected finding from genetic experiments in mice has given scientists a clearer picture of what makes mammals tick when it comes to fertility. With some exploration, the work could inspire a new wave of treatments for infertile humans; in some countries, up to one in ten human couples are unable to conceive. Fertility is controlled by the interactions of a complex series of hormones, one of which is luteinizing hormone (LH). Scientists genetically modified mice to lack the GalNAc-4-ST1 gene, which helps to clear LH from the blood. The resulting mice had 50% more pups, higher levels of testosterone and estrogen, matured earlier, and showed better care for their young. The modification seems to work because without the GalNAc-4-ST1 gene, the mice cannot remove a type of sugar linked to LH – which in turn means that the liver is less efficient at removing LH from the blood. - Journal of Clinical Investigation DOI: 10.1172/JCI32467, May 2008

Worrying new findings from experiments in mice suggest that the spread of nanotube technology could pose similar health risks to those caused by asbestos. When inhaled, asbestos fibres can lead to mesothelioma – a type of lung cancer – and some scientists are concerned that carbon nanotubes might do the same. Mice injected with nanotubes showed damage, inflammation and scarring from some of the longer fibres, comparable to that seen with asbestos fibres. Experiments where mice inhale nanotubes showed similar inflammation. Nanotubes had previously been assumed to be as safe as materials such as graphite. There is currently no proven link between nanotubes and mesothelioma, but they are already used in numerous everyday applications. Their widespread use is encouraging scientists to explore the matter further. - Nature Nanotechnology, online DOI: 10.1038/nnano.2008.111, 20 May 2008

Smallpox Drug Could Fight Common Cold

Immuno-compromised patients such AIDS victims, transplant recipients, and individuals with poorly functioning immune systems, often succumb to adenovirus infections – the same virus that causes the common cold. Up to four in five infections can be fatal, but a new treatment tested in hamsters could help to reduce that rate. CMX001 is an antiviral drug currently in testing to fight possible outbreaks of smallpox or monkeypox. Scientists discovered that not only were immuno-compromised Syrian hamsters a good animal model for the common cold, but also when treated with CMX001 they were able to fight off adenovirus infections. Although the findings are good news for patients, the treatment is some way off being used in humans. As well as needing further tests, the drug can currently only be given intravenously. - Proceedings of the National Academy of Sciences, online DOI: 10.1073/pnas.0800200105, 19 May 2008

Scientists have succeeded in creating rhesus macaques with Huntingdon’s disease, a genetic disorder causing physical and mental degradation in middle age. The work represents the first time a human genetic disorder has been reproduced in non-human primates, paving the way for advanced research into treatments and cures for the disease. The monkeys were genetically modified using a virus to insert the Huntingdon’s htt gene into unfertilized eggs. The eggs were then artificially fertilized, and implanted into surrogate mothers. Out of the two monkeys born which were healthy enough to make it through childhood, one began showing the tell-tale signs of Huntingdon’s disease at the age of 10 months. The other has no symptoms, but may develop them later. Currently, Huntingdon’s can be managed with drugs, but with only limited success. The presence of a primate model for the disease should allow scientists to find out much more accurately how the Huntingdon’s mutation affects our brains. - Nature, online DOI: 10.1038/nature06975, 18 May 2008

Scientists discovered the liver’s Ashwell receptor around 40 years ago, but have been clueless as to what it does until now. Working with mice, they have discovered it plays a crucial role in protecting the body from sepsis – a body-wide infection that can be fatal in over half of all cases. Sepsis often leads to death as the body literally destroys itself through a powerful immune response, rather than because of tissue damage due to the infection itself. When researchers created mice that had been genetically modified to lack the Ashwell receptor, they found that the mice were remarkably healthy – except that they died through sepsis much more often than normal mice. The study shows that Ashwell receptors play a vital role in preventing overactive clotting of the blood, which causes the blood to thicken and is responsible for up to half of all sepsis-related deaths. The findings could lead to new treatments for the condition. - Nature Medicine, online DOI: 10.1038/nm1760, 18 May 2008

Juiced Fruits Beat Cholesterol

Processed fruit could be even better for you than the raw version, according to new study carried out with hamsters. Scientists claim that although fruits like apples and grapes help to reduce atherosclerosis – the ‘furring’ of the arteries that leads to heart disease – the juices of the two fruits do it even more effectively. The researchers fed hamsters on a high-cholesterol diet, and divided them into groups which also ate or drank purple grape juice, apple juice, purple grapes, apples, or just had a normal diet with water. They found that fruit-eaters did better than those on the normal diet, but that the juice-drinkers had more protection against heart disease, with those drinking purple grape juice doing best of all. The team believes that the levels of phenols - which act as an anti-oxidant - are responsible for the improvements in the arteries, and hope that the work will inspire the use of fruit juices in a public health context. - Molecular Nutrition and Food Research DOI: 10.1002/mnfr.200700141, April 2008

MS Multiple sclerosis (MS) is a debilitating neurological disorder which affects up to one in 7000 people. Damage to the white matter of the brain causes increasing physical and eventually mental disability. There is currently no cure, but a mouse engineered to mimic the disease could be about to give hope to sufferers. Although there are a number of theories as to the underlying cause of the disease, one of the main mechanisms is the breakdown of brain tissue by the body’s own immune system. The collagenase-2 protein has been implicated in this breakdown, because it can be responsible for breaking down the blood-brain barrier, which allows the errant immune cells into the brain. The researchers found that in mice engineered to lack collagenase-2, and in mice treated with a drug that blocked its effects, the progression of the disease was considerably lessened. The protein could be a future target for treatments in humans. - Journal of Biological Chemistry DOI: 10.1074/jbc.M709522200, 4 April 2008

Scientists working with deer mice appear to have confirmed what we’ve been told for years by our mothers; the best medicine for fighting a cold is to keep well-fed. The researchers found how differing diet regimes affect the production of B-cells in the mice. B-cells are the immune system’s primary way of regulating the activity of antibodies, and are therefore its ‘memory’ cells. In those animals that had their food intake decreased by a third, levels of B-cells were significantly lower. The explanation for this is likely to be that maintaining immune system uses a lot of energy, so at of the year when food is scarce the body responds by reducing its activity. The result is that the immune system is less able to ‘remember’ how it fought past infections, and must fight new ones afresh. The research could have important consequences for human medicine, as vaccinations rely on B-cell activity. Ensuring that vaccinated people, especially in developing counties, have a good diet may be just as important as getting the vaccine itself to them. - Physical and Biochemical Zoology DOI: 10.1086/587090, 1 April 2008

One of the mutations which makes cells cancerous – the disabling of genes involved in cell-death – also makes them particularly hard to kill. It becomes impossible to flick a genetic switch and persuade the tumors to die. But scientists working with mice may have found a way to do the next best thing – putting the tumors to sleep. The research team found that the Id1 gene is essential to the growth of some types of breast cancer. When they stimulated the gene in healthy cells, the scientists found that the mice developed tumors. These tumors, with their high Id1 expression, became very aggressive and spread to the rest of the body. When the scientists inhibited the action of Id1 in an already-established tumor, they found that it halted their growth - effectively freezing them. Once they couldn’t grow, the immune system was able to break them down. In light of this, scientists hope that Id1 will prove a good target for future therapies in humans. - Proceedings of the National Academy of Sciences, Early Edition DOI: pnas.0801505105, 31 March 2008

Liver cirrhosis is the progressive loss of liver function due to the severe scarring of liver tissue, and usually results from alcoholism or hepatitis infection. It is thought this scarring is irreversible, and can eventually lead to death; currently, the only effective cure is a liver transplant. But scientists working with mice now believe they may have developed a new treatment. Hepatic stellate cells – a type of liver cell - are responsible for the scarring, which occurs when they secrete collagen in response to damage. The experimental cure works by wrapping a molecule that blocks collagen production in a vitamin A coating. The hepatic stellate cells are programmed to absorb vitamin A, and therefore also take up the collagen-blocking molecule. Disguised by the coating, the compound successfully stops further cirrhosis, and the research team found that the liver could then regenerate itself to compensate for existing damage. They hope that a drug for use in humans will be developed within a few years. - Nature Biotechnology, Online DOI: 10.1038/nbt1396, 30 March 2008

Although it is an important tool in treating cancer, chemotherapy can have a debilitating effect upon its recipients, including muscle wasting, fatigue, and loss of appetite. Because of this, doctors recommend that patients eat before the treatment – but new research in mice could turn that advice on its head. Scientists found that when they administered the chemotherapy drug cyclophosphamide to mice with brain tumors, healthy cells as well as cancerous cells were killed, with only a fifth of the cells surviving the treatment. But when the mice were starved before being given the treatment, four in five healthy cells survived, while the cancerous cells were killed off at the same rate as before. The researchers believe this effect is due to the ability of normal cells to slow down their metabolism during starvation, thus protecting themselves from damage by chemotherapy. Cancer cells, on the other hand, turn off that machinery in order to divide uncontrollably, so feel the full effects of the drugs. Scientists have stressed that further tests must be done to establish the mechanism in humans. - Proceedings of the National Academy of Sciences, Early Edition DOI: 10.1073/pnas.0708100105, 30 March 2008

Thanks to new understanding of the disease in mice, a new treatment for cystic fibrosis (CF) may be on the cards. One of the leading causes of death in CF is repeated infection of the lungs by bacteria, which eventually cause so much damage that only a complete lung transplant can save the individual. The infections had previously been thought to occur due to the bacteria evading the immune system in the thick CF mucous. Now, scientists believe that the infections may actually be due to the inability of CF sufferers to break down ceramide, a type of fat. When ceramide builds up, it leads to cell-death and inflammation, thus creating the conditions for a bacterial infection to take a foothold. Scientists have found that when CF-mice are given a drug to block the production of ceramide, they have lower levels of the fat, which results in fewer infections and healthier mice. The scientists hope that an appropriate dose of the drugs will have a similar effect in humans, without blocking ceramide production completely. - Nature Medicine, Online DOI: 10.1038/nm1748, 30 March 2008

The modern obesity epidemic is often blamed on the human sweet tooth; we enjoy the taste of high-calorie food, and can’t get enough of it. But new research in genetically modified mice suggests that the predilection might go further than previously anticipated. The experimental mice had their trpm5 genes – without which they cannot taste sugar – knocked out, so were ‘sweet-blind’. They were then given the choice of two drinks; sugared water, or water with a low-calorie artificial sweetener dissolved in it. Despite not being able to taste any difference between the two, they developed a strong preference for the high-calorie sugared water. There seems to be another pathway, apart from taste, that acts as a reward mechanism for eating calorific food. If the findings are applicable to humans, they could have implications for weight-loss efforts – particularly if a way were found to block the reward pathway. - Neuron DOI: 10.1016/j.neuron.2008.01.032, 27 March 2008

As governments around the world continue to prepare for a possible outbreak of H5N1 bird flu in humans, we are still searching for an effective vaccine for the strain. Scientists hope this may be about to change after experiments in mice yielded promising results. The virus is made up of a number of different proteins, and these proteins are in turn composed of a variety of ‘domains’. One of the domains of the virus’ M2 protein is called the cytoplasmic tail. Previous research in a different influenza strain had shown that deleting this cytoplasmic tail resulted in a growth defect in the viruses, suggesting that it plays a vital role in replication. Scientists succeeded in mutating the same protein in the H5N1 virus, before vaccinating mice with the mutant virus. They found that when the vaccinated mice were then exposed to a lethal dose of normal H5N1, the virus could not replicate, and the mice fought off the infection. The hope is that this research could form the basis of a human vaccine against the ‘flu strain. - Journal of Virology DOI: 10.1128/JVI.01899-07, March 2008

Researchers have found a new way to encourage the growth of blood vessels in mice. The finding could help treat heart disease and cancer in future. The scientists found that when tissue is starved of oxygen, a molecule called PGC-1alpha senses the change and encourages the body to grow new blood vessels in the affected area to restore oxygen flow. It is already known that another molecular pathway, involving vascular endothelial growth factor (VEGF), can have a similar effect. But mice seem to need both pathways for the best response to oxygen starvation – GM mice lacking PGC-1alpha were less able to grow new blood vessels. A number of anticancer treatments work by stopping the growth of new blood vessels feeding the tumors. Until now, these therapies have focused on the VEGF pathway. The new study suggests that if such therapies also targeted PGC-1alpha, they might be more effective. - Nature DOI: 10.1038/nature06613, 21 February 2008

Brain cells grown from human embryonic stem cells can help repair brain damage in rats after a stroke. Researchers encouraged human embryonic stem cells to develop into neural stem cells. When these stem cells were transplanted into the rats, they grew into brain cells to replace those lost during the stroke. Some of the rats had lost the power of control in their limbs as a result of the stroke, but after treatment some of this control was recovered. The researchers think a similar technique could be used in patients within five years. - PLoS ONE DOI: 10.1371/journal.pone.0001644, 20 February 2008

Growing Beta Cells

Researchers have turned human embryonic stem cells into functioning pancreatic beta cells in mice, in a study that could help treat type-1 diabetics. Type-1 diabetics have no insulin-producing beta cells and cannot respond to changes in blood sugar. Scientists have considered turning embryonic stem cells into beta cells to treat diabetics, but they have had no success until now. Researchers treated embryonic stem cells with a chemical cocktail that encouraged them to become pancreatic endoderm cells, the cells present in the foetus that go on to form the pancreas. When these immature pancreatic cells were injected into the pancreas of diabetic mice, they developed into beta cells and began producing insulin. After two months, the beta cells were responding normally to rises in blood sugar after feeding. Tests in humans could begin as soon as safety considerations have been considered. - Nature Biotechnology DOI: 10.1038/nbt1393, 20 February 2008

Gene Therapy for Brain Cancer

Research with rats suggests that gene therapy could be used to treat glioblastoma multiforme, a common and fatal brain cancer. Researchers removed all of the dangerous genes from a virus and used it to deliver two key proteins directly to cancer cells in the brain. One of the proteins acts as a marker to encourage the body’s immune cells to attack the cancer cells. The other protein fights the cells from the inside – it becomes toxic inside the tumor and kills the cancer cells. Rats with the brain cancer had their condition reversed using the gene therapy. The researchers are now about to begin human trials using the therapy. - Molecular Therapy , 19 February 2008

Controlling the amount of nitric oxide in tumors could help improve the effectiveness of anti-cancer treatments, according to a study with mice. As tumors grow, new blood vessels develop to feed them with oxygen. But the new vessels are leaky, making them unsuitable for delivering chemotherapy drugs to the tumor. Drugs that suppress the growth of new blood vessels in tumors improve the effectiveness of chemotherapy drugs. Scientists think this is because the vessel growth-suppressing drugs encourage existing blood vessels to develop properly without leaks, making them more effective for delivering anti-cancer drugs. Blood vessel growth is controlled by nitric oxide, so restricting the amount of nitric oxide around a tumor could also encourage existing blood vessels to develop properly. When researchers modified cancer cells to produce less nitric oxide and injected the cells into mice, the tumors that developed were fed by well-developed blood vessels that were suitable for chemotherapy treatment. - Nature Medicine, online DOI: 10.1038/nm1730, 17 February 2008

First Chikungunya Animal Model

Researchers have created a mouse model for the chikungunya virus (CHIKV), a new virus that led to an epidemic in the Indian Ocean in 2005. The virus leads to fever, joint pains and a skin rash, but the factors responsible for the symptoms are unclear. The new model could help explain how the disease develops. Researchers deleted a gene for a protein that plays an important role in the mouse antiviral response. When one copy of the gene was deleted, the mice mimicked the benign form of CHIKV, but with both copies removed the mice mimicked the severe form of disease. Using the mouse model, the researchers have shown that CHIKV begins in the liver and then spreads to the joints and muscles. They expect the model to help in the search for an effective treatment. - PLoS Pathogens DOI: 10.1371/journal.ppat.0040029, 15 February 2008

Mice missing a gene could help in the identification of new treatments for bipolar disorder. Researchers discovered that mice missing the gene, NR-2E1, are prone to attack and kill other mice. Now they have found that the gene is also mutated in patients with bipolar disorder (formerly called manic depression). The gene seems to regulate the development of the front region of the brain, which is involved in decision-making. It suggests that bipolar disorder results from developmental problems. Next, researchers will take different varieties of NR-2E1 from patients and study their action in mice to see which lead to most aggressive behavior. - American Journal of Medical Genetics Part B DOI: 10.1002/ajmg.b.30696, 18 January 2008

Controlling the amount of cholesterol in the brain could help delay the onset of Alzheimer’s disease, according to research with mice. Researchers discovered the enzyme ABCA1 in 2001, and found that it controls the level of cholesterol in the blood. But it also seems to prevent the formation of the plaques that are common in the brains of Alzheimer’s patients. GM mice lacking the enzyme produce many more plaques than normal. Now, researchers have produced GM mice with high levels of ABCA1 in the brain. When these mice were bred with mice prone to Alzheimer’s, the offspring developed the disease at a slower rate than normal. Drugs to increase the level of ABCA1 could help treat Alzheimer’s. Such drugs already exist, but they also lead to unwanted fat build-up in the liver. - Journal of Clinical Investigation, online DOI: 10.1172/JCI33622, 17 January 2008

Research with mice suggests that melanoma arises because of a small population of cancer stem cells. Scientists know that the protein ABCB5 is found on the surface of some skin cells and helps skin cancers resist treatment. They thought that the protein could help identify cancer stem cells. The researchers took human melanoma cells and separated those cells producing the protein. When they injected these cells into mice, over half of the mice developed tumors. But when the researchers injected mice with the human melanoma cells lacking ABCB5, only one mouse of 23 developed a tumor. The study suggests that ABCB5 can act as a tool to identify – and ultimately eliminate – the dangerous cancer stem cells, which are capable of re-growing a tumor from scratch. - Nature DOI: 10.1038/nature06489, 17 January 2008

Researchers have identified a better method of alleviating chronic pain while avoiding side effects such as drowsiness, following a study with mice. The spinal cord helps to organize pain signals, and prevents many from reaching the brain through the action of a molecule called GABA. Medicines such as diazepam (valium) increase the activity of GABA, but they lead to addiction and drowsiness. Diazepam is an indiscriminate drug, say the researchers, because it interacts with four different GABA receptors. Now, research with mice suggests a therapy can be just as potent by targeting just two of those receptors. Researchers produced GM mice in which just two of the receptors could be targeted by drugs, and found that they could still alleviate pain in these mice. New medicines to target a narrower arrange of GABA receptors could avoid unwanted side effects. The next step is to identify the drugs that will work in humans. - Nature DOI: 10.1038/nature06493, 17 January 2008

Research with mice suggests that some probiotic bacteria in food can cause metabolic changes in the body and prevent weight gain. Scientists fed a group of mice on a solution containing one species of the bacteria found in yoghurt. A second group of mice was given a saline solution instead. After two weeks, both groups of mice still had very similar populations of gut microbes. But the metabolic profiles had changed. The mice receiving yoghurt bacteria produced less bile acid. Because bile acid normally helps emulsify fat, which helps the body absorb fat from food, the mice producing lower quantities of the acid were less efficient at absorbing fat, and so remained thin. The researchers are excited to find that it is possible to alter metabolism by making small changes to gut bacteria. - Molecular Systems Biology, online DOI: 10.1038/msb4100190,15 January 2008

Industrial air pollution can cause defects in sperm, research with mice suggests. Researchers reared one group of mice downwind of two steel mills and a busy main road. A second group was given filtered air. When the researchers studied the sperm of mice in both groups three weeks later, they found more physical damage, in the form of DNA strand breaks, in the mice breathing polluted air. After 16 weeks, the mice breathing polluted air produced sperm with 60% more DNA mutations than the mice breathing normal air. Air pollution is already linked to breathing difficulties, but this is one of the first studies to examine its effect on fertility. - Proceedings of the National Academy of Sciences, online DOI: 10.1073/pnas.0705896105, 14 January 2008

Hair to Heal Nerves

Research with mice suggests that human hair could hold the key to regenerating damaged nerves. Following nerve damage, it is difficult to get the broken ends of a nerve to grow back together again. To help the process, surgeons use nerve guidance conduits – microscopic tubes which they attach between damaged nerve ends that give the nerve a scaffolding to grow around. But the conduits work only over short distances, and nerve regeneration is a slow process. Now, researchers have extracted keratin protein from human hair and shown that, when the conduits are filled with the protein, nerve regeneration speeds up. Keratin acts on the Schwann cells that help in the healing process. When the researchers tried to repair damaged nerves in mice using keratin, they saw nerve re-growth in all cases. Given enough healing time, the researchers think that the nerve re-growth could help the mice recover full muscle control. - Biomaterials DOI: 10.1016/j.biomaterials.2007.08.023, 1 January 2008

Research has identified a drug therapy that could help treat Batten disease, a fatal childhood neurodegenerative disease. There are currently no treatments for the disease, and children gradually lose motor skills, sight and reasoning. Now, researchers have succeeded in reversing some of the symptoms of disease in mice. They already know that mice with the disease have unusually sensitive brain receptor cells in the cerebellum, a brain region involved in sense perception and motor control. They gave mice with the disease a chemical to dull the activity of the nerve receptors. The mice stopped deteriorating and began to improve their coo - Experimental Neurology DOI: 10.1016/j.expneurol.2007.09.012, January 2008